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group_4_presentation_2_-_chronic_obstructive_pulmonary_disease_copd [2016/11/03 18:25]
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group_4_presentation_2_-_chronic_obstructive_pulmonary_disease_copd [2018/01/25 15:18] (current)
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 ===== Introduction ===== ===== Introduction =====
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-<box width classes round white centre|>​{{:​summary_of_pathways_and_candidate_genes_involved_in_copd.png|}}</​box| Figure : Summary of Pathways and Candidate Genes Involved in COPD. Retrieved from:+<box width classes round white centre|>​{{:​summary_of_pathways_and_candidate_genes_involved_in_copd.png|}}</​box| Figure ​3: Summary of Pathways and Candidate Genes Involved in COPD. Retrieved from:
 http://​citeseerx.ist.psu.edu/​viewdoc/​download?​doi=10.1.1.629.4676&​rep=rep1&​type=pdf>​ http://​citeseerx.ist.psu.edu/​viewdoc/​download?​doi=10.1.1.629.4676&​rep=rep1&​type=pdf>​
  
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-<box width classes round white centre|>​{{:​a._normal_small_airway_b._abnormal_small_airway_exhibiting_airway_remodeling_in_copd._berge_et_al._2011_.png|}}</​box| Figure : A. Normal Small Airway, B. Abnormal Small Airway Exhibiting Airway Remodeling in COPD. Modified from: Berge et al. (2011)>+<box width classes round white centre|>​{{:​a._normal_small_airway_b._abnormal_small_airway_exhibiting_airway_remodeling_in_copd._berge_et_al._2011_.png|}}</​box| Figure ​5: A. Normal Small Airway, B. Abnormal Small Airway Exhibiting Airway Remodeling in COPD. Modified from: Berge et al. (2011)>
  
  
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-<box width classes round white centre|>​{{:​spirometry_traces_representing_healthy_patients_and_copd_patients.png|}}</​box| Figure : Spirometry Traces Representing Healthy Patients and COPD Patients. Retrieved from: http://​www.thinkcopdifferently.com/​en/​About-COPD/​Diagnosing-COPD/​Spirometric-assessment>​+<box width classes round white centre|>​{{:​spirometry_traces_representing_healthy_patients_and_copd_patients.png|}}</​box| Figure ​6: Spirometry Traces Representing Healthy Patients and COPD Patients. Retrieved from: http://​www.thinkcopdifferently.com/​en/​About-COPD/​Diagnosing-COPD/​Spirometric-assessment>​
  
  
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 Across North America, pulmonary rehabilitation has become an extremely popular method for long-term management of COPD (Goldstein et al., 1994). It aims to manage and improve some of the disabilities that are associated with COPD, such as decreased motor function and weight loss (Goldstein et al., 1994). There are three facets of pulmonary rehabilitation are: the multidisciplinary nature of, individualized programs and attention to physical and social function (Ries & Squier, 1996). The collaboration between various kinds health care professionals makes pulmonary rehabilitation very successful because it encompasses a variety of health care fields. Individuals involved include: physicians, nurses, occupational therapists, psychologists,​ nutritionists and exercise specialists. (Ries & Squier, 1996). Additionally,​ the emphasis on an individualized rehabilitation plans leads to successful outcomes because patients are able to focus on the areas that they need to develop the most (Ries & Squier, 1996). Finally, by focusing on both the physical and social function of these individuals,​ pulmonary rehabilitation allows patients to work on emotional issues. This aspect has been correlated with better outcomes in physical symptoms, such as lung function and exercise tolerance (Ries & Squier, 1996). ​ Across North America, pulmonary rehabilitation has become an extremely popular method for long-term management of COPD (Goldstein et al., 1994). It aims to manage and improve some of the disabilities that are associated with COPD, such as decreased motor function and weight loss (Goldstein et al., 1994). There are three facets of pulmonary rehabilitation are: the multidisciplinary nature of, individualized programs and attention to physical and social function (Ries & Squier, 1996). The collaboration between various kinds health care professionals makes pulmonary rehabilitation very successful because it encompasses a variety of health care fields. Individuals involved include: physicians, nurses, occupational therapists, psychologists,​ nutritionists and exercise specialists. (Ries & Squier, 1996). Additionally,​ the emphasis on an individualized rehabilitation plans leads to successful outcomes because patients are able to focus on the areas that they need to develop the most (Ries & Squier, 1996). Finally, by focusing on both the physical and social function of these individuals,​ pulmonary rehabilitation allows patients to work on emotional issues. This aspect has been correlated with better outcomes in physical symptoms, such as lung function and exercise tolerance (Ries & Squier, 1996). ​
  
-<box width classes round white centre|>​{{:​nutrition.png|}}</​box| Retrieved from: http://​blog.copdstore.com/​the-official-guide-to-copd-nutrition>​+<box width classes round white centre|>​{{:​nutrition.png|}}</​box| ​Figure 7: Foods Full of Nutrition. ​Retrieved from: http://​blog.copdstore.com/​the-official-guide-to-copd-nutrition>​
  
  
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-<box width classes round white centre|>​{{:​pulmonary_rehabilitation_in_action.png|}}</​box| Retrieved from: http://​drvijaynair.8m.com/​ >+<box width classes round white centre|>​{{:​pulmonary_rehabilitation_in_action.png|}}</​box| ​Figure 8: Pulmonary Rehabilitation in Action. ​Retrieved from: http://​drvijaynair.8m.com/​ >
  
  
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-<box width classes round white centre|>​{{:​significant_improvement_in_exercise_improvement.png|}}</​box| Figure : Significant improvement in exercise endurance, for up to 3 months, in individuals who participated in 6 weeks of pulmonary rehabilitation. Modified from: Berry et al. (1999)>+<box width classes round white centre|>​{{:​significant_improvement_in_exercise_improvement.png|}}</​box| Figure ​9: Significant improvement in exercise endurance, for up to 3 months, in individuals who participated in 6 weeks of pulmonary rehabilitation. Modified from: Berry et al. (1999)>
  
  
 Furthermore,​ a study done by Lacasse et al. (2006), showed significant improvements with the participation in pulmonary rehabilitation in other symptoms common to COPD patients as well. It was proven that pulmonary rehabilitation relieved symptoms of dyspnea (labored breathing) and fatigue, which is common found in COPD patients due to the muscle loss and increased energy expenditure of movement (Lacasse et al. 2006). Additionally,​ improvements to the emotional state of COPD patients were shown to enhance an individual’s sense of mastery and control over their condition (Lacasee et al., 2006). Results of this study are shown below. After much research, the significant yield of results illustrate why pulmonary rehabilitation is a crucial component in the long-term management of COPD.  Furthermore,​ a study done by Lacasse et al. (2006), showed significant improvements with the participation in pulmonary rehabilitation in other symptoms common to COPD patients as well. It was proven that pulmonary rehabilitation relieved symptoms of dyspnea (labored breathing) and fatigue, which is common found in COPD patients due to the muscle loss and increased energy expenditure of movement (Lacasse et al. 2006). Additionally,​ improvements to the emotional state of COPD patients were shown to enhance an individual’s sense of mastery and control over their condition (Lacasee et al., 2006). Results of this study are shown below. After much research, the significant yield of results illustrate why pulmonary rehabilitation is a crucial component in the long-term management of COPD. 
  
-<box width classes round white centre|>​{{:​improvement_of_symptoms.png|}}</​box| Figure : Illustration of the improvement of symptoms, which are common in COPD patients, with the participation in pulmonary rehabilitation. Modified from: Lacasse et al. (2006)>+<box width classes round white centre|>​{{:​improvement_of_symptoms.png|}}</​box| Figure ​10: Illustration of the improvement of symptoms, which are common in COPD patients, with the participation in pulmonary rehabilitation. Modified from: Lacasse et al. (2006)>
  
  
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 Bronchodilators are a class of medications that are widely used to treat COPD and aid in preventing airflow obstruction in COPD patients (Shim, 1989). These drugs provide relief of some symptoms commonly associated with COPD, such as dyspnea or decreased exercise tolerance, through the relaxation of smooth muscle that line airways (Barnes, 1995). Due to the increase build-up of smooth muscle in COPD patients and subsequent impairment of lung function, these bronchodilators are extremely important in the prevention/​reduction of airway obstruction (Berge et al., 2011). The two main bronchodilators used in the treatment of COPD are beta-agonist’s and anti-cholinergic’s (Barnes, 1995). Beta-agonist’s are the most widely used bronchodilator typically used to treat COPD patients (Barnes, 1995). Beta-agonist’s act by binding to the adrenergic receptors on smooth muscle cells and cause an increase of cyclic-AMP (cAMP), a secondary messenger, within the smooth muscle cell. The increase in cAMP causes an intra-cellular cascade that ultimately leads to a relaxation of the smooth muscle surrounding the airway and thus causing bronchodilation (Tashkin & Fabbri, 2010). Long-acting beta-agonist’s in specific, such as formoterol or salmeterol, have been proven to more effectively than regular beta-agonist medications,​ primarily due to their rapid onset and long duration of action (Barnes, 1995). ​ Bronchodilators are a class of medications that are widely used to treat COPD and aid in preventing airflow obstruction in COPD patients (Shim, 1989). These drugs provide relief of some symptoms commonly associated with COPD, such as dyspnea or decreased exercise tolerance, through the relaxation of smooth muscle that line airways (Barnes, 1995). Due to the increase build-up of smooth muscle in COPD patients and subsequent impairment of lung function, these bronchodilators are extremely important in the prevention/​reduction of airway obstruction (Berge et al., 2011). The two main bronchodilators used in the treatment of COPD are beta-agonist’s and anti-cholinergic’s (Barnes, 1995). Beta-agonist’s are the most widely used bronchodilator typically used to treat COPD patients (Barnes, 1995). Beta-agonist’s act by binding to the adrenergic receptors on smooth muscle cells and cause an increase of cyclic-AMP (cAMP), a secondary messenger, within the smooth muscle cell. The increase in cAMP causes an intra-cellular cascade that ultimately leads to a relaxation of the smooth muscle surrounding the airway and thus causing bronchodilation (Tashkin & Fabbri, 2010). Long-acting beta-agonist’s in specific, such as formoterol or salmeterol, have been proven to more effectively than regular beta-agonist medications,​ primarily due to their rapid onset and long duration of action (Barnes, 1995). ​
  
-<box width classes round white centre|>​{{:​action_of_beta-agonists.png|}}</​box| Figure : Mechanism of Action of Beta-Agonists>​+<box width classes round white centre|>​{{:​action_of_beta-agonists.png|}}</​box| Figure ​13: Mechanism of Action of Beta-Agonists>​
  
 The other kind of bronchodilator used are anti-cholinergic’s,​ also known as muscarinic antagonists. These not used as often as beta-agonist’s but have been shown to aid in improvement of airway flow in COPD patients as well (Barnes, 1995). Anti-cholinergic’s act by blocking the binding of acetylcholine,​ which is released from the pre-synaptic cleft of a neuron, to the smooth muscle acetylcholine receptor. By blocking the binding, anti-cholinergic’s are able to prevent bronchoconstriction (Tashkin & Fabbri, 2010).  ​ The other kind of bronchodilator used are anti-cholinergic’s,​ also known as muscarinic antagonists. These not used as often as beta-agonist’s but have been shown to aid in improvement of airway flow in COPD patients as well (Barnes, 1995). Anti-cholinergic’s act by blocking the binding of acetylcholine,​ which is released from the pre-synaptic cleft of a neuron, to the smooth muscle acetylcholine receptor. By blocking the binding, anti-cholinergic’s are able to prevent bronchoconstriction (Tashkin & Fabbri, 2010).  ​
  
  
-<box width classes round white centre|>​{{:​action_of_anti-cholinergics.png|}}</​box| Figure : Action of Anti-Cholinergics>​+<box width classes round white centre|>​{{:​action_of_anti-cholinergics.png|}}</​box| Figure ​14: Action of Anti-Cholinergics>​
  
  
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 Studies have shown the long-acting beta-agonist’s (LABAs), such as formoterol, are the best course of medical treatments for individuals with COPD (Rossi, Khirani & Cazzola, 2008). These LABAs are more effective due to their rapid onset and prolonged duration (Barnes, 1995). When used, COPD patients saw improvement with common symptoms, such as dyspnea and decreased exercise tolerance, within minutes-hours after ingestion. Additionally,​ these drugs also helped improved lung function, reduce exacerbations and overall improve the health status of symptomatic patients with moderate-severe COPD (Rossi, Khirani & Cazzola, 2008). In a clinical study done by Van Noord et al. (2005), results showed that the efficacy of LABAs improved with the combined use of anti-cholinergic drugs. These results were only found in patients with severe COPD and only for the first 12-24 hours after ingestion (Van Noord et al., 2005). ​ Studies have shown the long-acting beta-agonist’s (LABAs), such as formoterol, are the best course of medical treatments for individuals with COPD (Rossi, Khirani & Cazzola, 2008). These LABAs are more effective due to their rapid onset and prolonged duration (Barnes, 1995). When used, COPD patients saw improvement with common symptoms, such as dyspnea and decreased exercise tolerance, within minutes-hours after ingestion. Additionally,​ these drugs also helped improved lung function, reduce exacerbations and overall improve the health status of symptomatic patients with moderate-severe COPD (Rossi, Khirani & Cazzola, 2008). In a clinical study done by Van Noord et al. (2005), results showed that the efficacy of LABAs improved with the combined use of anti-cholinergic drugs. These results were only found in patients with severe COPD and only for the first 12-24 hours after ingestion (Van Noord et al., 2005). ​
  
-<box width classes round white centre|>​{{:​improvement_of_lung_capacity.png|}}</​box| Figure : Improvement of lung capacity, within the first 12-24 hours, in individuals with severe COPD after the ingestion of both long-acting beta-agonist’s and anticholingeric medications. Modified from: Van Noord et al. (2005)>+<box width classes round white centre|>​{{:​improvement_of_lung_capacity.png|}}</​box| Figure ​15: Improvement of lung capacity, within the first 12-24 hours, in individuals with severe COPD after the ingestion of both long-acting beta-agonist’s and anticholingeric medications. Modified from: Van Noord et al. (2005)>
  
  
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 ===== References ===== ===== References =====
-Barnes, P. J. (1995). Bronchodilators:​ basic pharmacology. In Chronic obstructive pulmonary disease (pp. 391-417). Springer US.+1. Barnes, P. J. (1995). Bronchodilators:​ basic pharmacology. In Chronic obstructive pulmonary disease (pp. 391-417). Springer US.
  
-Bauer, J., Biolo, G., Cederholm, T., Cesari, M., Cruz-Jentoft,​ A. J., Morley, J. E., ... & Visvanathan,​ R. (2013). Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. Journal of the American Medical Directors Association,​ 14(8), 542-559.+2. Bauer, J., Biolo, G., Cederholm, T., Cesari, M., Cruz-Jentoft,​ A. J., Morley, J. E., ... & Visvanathan,​ R. (2013). Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. Journal of the American Medical Directors Association,​ 14(8), 542-559.
  
-Berge, M. V., Hacken, N. H., Cohen, J., Douma, W. R., & Postma, D. S. (2011). Small Airway Disease in Asthma and COPD. Chest, 139(2), 412-423. doi:​10.1378/​chest.10-1210+3. Berge, M. V., Hacken, N. H., Cohen, J., Douma, W. R., & Postma, D. S. (2011). Small Airway Disease in Asthma and COPD. Chest, 139(2), 412-423. doi:​10.1378/​chest.10-1210
  
-Bourdin, A., Burgel, P., Chanez, P., Garcia, G., Perez, T., & Roche, N. (2009, September 5). Recent advances in COPD: Pathophysiology,​ respiratory physiology and clinical aspects, including comorbidities. European Respiratory Review, 18(114), 198-212. Doi: 10.1183/​09059180.00005509.+4. Bourdin, A., Burgel, P., Chanez, P., Garcia, G., Perez, T., & Roche, N. (2009, September 5). Recent advances in COPD: Pathophysiology,​ respiratory physiology and clinical aspects, including comorbidities. European Respiratory Review, 18(114), 198-212. Doi: 10.1183/​09059180.00005509.
  
-Brug, J., Schols, A., & Mesters, I. (2004). Dietary change, nutrition education and chronic obstructive pulmonary disease. Patient education and counseling, 52(3), 249-257.+5. Brug, J., Schols, A., & Mesters, I. (2004). Dietary change, nutrition education and chronic obstructive pulmonary disease. Patient education and counseling, 52(3), 249-257.
  
-Cambach, W., Wagenaar, R. C., Koelman, T. W., van Keimpema, T., & Kemper, H. C. (1999). The long-term effects of pulmonary rehabilitation in patients with asthma and chronic obstructive pulmonary disease: a research synthesis. Archives of physical medicine and rehabilitation,​ 80(1), 103-111.+6. Cambach, W., Wagenaar, R. C., Koelman, T. W., van Keimpema, T., & Kemper, H. C. (1999). The long-term effects of pulmonary rehabilitation in patients with asthma and chronic obstructive pulmonary disease: a research synthesis. Archives of physical medicine and rehabilitation,​ 80(1), 103-111.
  
-Castaldi, P., et al. (2010). The COPD genetic association compendium: a comprehensive online database of COPD genetic associations. Human Molecular Genetis. 19 (3), 526-534. Doi:​10.1093/​hmg/​ddp519+7. Castaldi, P., et al. (2010). The COPD genetic association compendium: a comprehensive online database of COPD genetic associations. Human Molecular Genetis. 19 (3), 526-534. Doi:​10.1093/​hmg/​ddp519
    
-Chung, K. F. (2005, June 22). The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease. Proceedings of the American Thoracic Society, 2(4), 347-354. doi:​10.1513/​pats.200504-028sr.+8. Chung, K. F. (2005, June 22). The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease. Proceedings of the American Thoracic Society, 2(4), 347-354. doi:​10.1513/​pats.200504-028sr.
  
-DeMeo, D., et al. (2009). Integration of genomic and genetic approaches implicates IREB2 as a COPD susceptibility gene. American journal of human genetics. 85 (4), 493-502. Doi:​10.1016/​j.ajhg.2009.09.004+9. DeMeo, D., et al. (2009). Integration of genomic and genetic approaches implicates IREB2 as a COPD susceptibility gene. American journal of human genetics. 85 (4), 493-502. Doi:​10.1016/​j.ajhg.2009.09.004
  
-Goldstein, R. S., Gort, E. H., Avendano, M. A., Stubbing, D., & Guyatt, G. H. (1994). Randomised controlled trial of respiratory rehabilitation. The Lancet,​344(8934),​ 1394-1397.+10. Goldstein, R. S., Gort, E. H., Avendano, M. A., Stubbing, D., & Guyatt, G. H. (1994). Randomised controlled trial of respiratory rehabilitation. The Lancet,​344(8934),​ 1394-1397.
  
-Hancock, D., et al. (2010). Meta-analyses of genome-wide association studies identify multiple loci associated with pulmonary function. Nature genetics. 42 (1), 45-52. Doi:​10.1038/​ng.500+11. Hancock, D., et al. (2010). Meta-analyses of genome-wide association studies identify multiple loci associated with pulmonary function. Nature genetics. 42 (1), 45-52. Doi:​10.1038/​ng.500
    
-Hautamaki, R., et al. (1997). Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. Science (New York, N.Y.). 277 (5334), 2002-4. Doi:​10.1126/​science.277.5334.2002+12. Hautamaki, R., et al. (1997). Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. Science (New York, N.Y.). 277 (5334), 2002-4. Doi:​10.1126/​science.277.5334.2002
    
-Joos, J., Pare, P., Sandford, A. (2002). Genetic risk factors for chronic obstructive pulmonary disease. Wolters Kluwer Health. 8 (2), 87-97. Doi: 2002/​03/​smw-09752+13. Joos, J., Pare, P., Sandford, A. (2002). Genetic risk factors for chronic obstructive pulmonary disease. Wolters Kluwer Health. 8 (2), 87-97. Doi: 2002/​03/​smw-09752
  
-Ko, F. & Hui, D. (2012). Air pollution and chronic obstructive pulmonary disease. Respirology. 17 (3), 395-401. Doi: 10.1111/​j.1440-1843.2011.02112.x+14. Ko, F. & Hui, D. (2012). Air pollution and chronic obstructive pulmonary disease. Respirology. 17 (3), 395-401. Doi: 10.1111/​j.1440-1843.2011.02112.x
  
-MacNee, W. (2006, May 20). ABC of chronic obstructive pulmonary disease: Pathology, pathogenesis,​ and pathophysiology. Bmj, 332(7551), 1202-1204. doi:​10.1136/​bmj.332.7551.1202.+15. MacNee, W. (2006, May 20). ABC of chronic obstructive pulmonary disease: Pathology, pathogenesis,​ and pathophysiology. Bmj, 332(7551), 1202-1204. doi:​10.1136/​bmj.332.7551.1202.
  
-Matheson, M., et al. (2005). Biological dust exposure in the workplace is a risk factor for chronic obstructive pulmonary disease. Thorax. 60 (8), 645-51. Doi: 10.1136/​thx.2004.035170+16. Matheson, M., et al. (2005). Biological dust exposure in the workplace is a risk factor for chronic obstructive pulmonary disease. Thorax. 60 (8), 645-51. Doi: 10.1136/​thx.2004.035170
  
-Paknikar S. (2013). Increased Airway Resistance in COPD Occurs Due to Loss or Narrowing of Small Airways. http://​www.medindia.net/​news/​healthinfocus/​increased-airway-resistance-in-copd-occurs-due-to-loss-or-narrowing-of-small-airways-92858-1.htm+17. Paknikar S. (2013). Increased Airway Resistance in COPD Occurs Due to Loss or Narrowing of Small Airways. http://​www.medindia.net/​news/​healthinfocus/​increased-airway-resistance-in-copd-occurs-due-to-loss-or-narrowing-of-small-airways-92858-1.htm
  
-Pendas, A., et al. (1996). Fine physical mapping of the human matrix metalloproteinase genes clustered on chromosome 11q22.3. Genomics. 37 (2), 266-8. Doi: 10.1006/​geno.1996.0557+18. Pendas, A., et al. (1996). Fine physical mapping of the human matrix metalloproteinase genes clustered on chromosome 11q22.3. Genomics. 37 (2), 266-8. Doi: 10.1006/​geno.1996.0557
  
-Pillai, S., et al. (2009). A genome-wide association study in chronic obstructive pulmonary disease (COPD): identification of two major susceptibility loci. PLoS genetics. 5 (3). Doi: 10.1371/​journal.pgen.1000421+19. Pillai, S., et al. (2009). A genome-wide association study in chronic obstructive pulmonary disease (COPD): identification of two major susceptibility loci. PLoS genetics. 5 (3). Doi: 10.1371/​journal.pgen.1000421
  
-Ries, A. L., & Squier, H. C. (1996). The team concept in pulmonary rehabilitation. Lung Biology in Health and Disease, 91, 55-66.+20. Ries, A. L., & Squier, H. C. (1996). The team concept in pulmonary rehabilitation. Lung Biology in Health and Disease, 91, 55-66.
  
-Ries, A. L., Bauldoff, G. S., Carlin, B. W., Casaburi, R., Emery, C. F., Mahler, D. A., ... & Herrerias, C. (2007). Pulmonary rehabilitation:​ joint ACCP/AACVPR evidence-based clinical practice guidelines. CHEST Journal,​131(5_suppl),​ 4S-42S. ​+21. Ries, A. L., Bauldoff, G. S., Carlin, B. W., Casaburi, R., Emery, C. F., Mahler, D. A., ... & Herrerias, C. (2007). Pulmonary rehabilitation:​ joint ACCP/AACVPR evidence-based clinical practice guidelines. CHEST Journal,​131(5_suppl),​ 4S-42S. ​
  
-Rossi, A., Khirani, S., & Cazzola, M. (2008). Long-acting β2-agonists (LABA) in chronic obstructive pulmonary disease: efficacy and safety. International Journal of Chronic Obstructive Pulmonary Disease, 3(4), 521–529.+22. Rossi, A., Khirani, S., & Cazzola, M. (2008). Long-acting β2-agonists (LABA) in chronic obstructive pulmonary disease: efficacy and safety. International Journal of Chronic Obstructive Pulmonary Disease, 3(4), 521–529.
  
-Schols, A. M., Slangen, J. O. S., Volovics, L., & Wouters, E. F. (1998). Weight loss is a reversible factor in the prognosis of chronic obstructive pulmonary disease. American journal of respiratory and critical care medicine, 157(6), 1791-1797.+23. Schols, A. M., Slangen, J. O. S., Volovics, L., & Wouters, E. F. (1998). Weight loss is a reversible factor in the prognosis of chronic obstructive pulmonary disease. American journal of respiratory and critical care medicine, 157(6), 1791-1797.
    
-Shim, C. (1989). Response to bronchodilators. Clinics in chest medicine, 10(2), 155-164.+24. Shim, C. (1989). Response to bronchodilators. Clinics in chest medicine, 10(2), 155-164.
    
-Smith, C. & Harrison, D. (1997). Association between polymorphism in gene for microsomal epoxide hydrolase and susceptibility to emphysema. The Lancet. 350 (9078), 630-633. Doi: 10.1016/​S0140-6736(96)08061-0+25. Smith, C. & Harrison, D. (1997). Association between polymorphism in gene for microsomal epoxide hydrolase and susceptibility to emphysema. The Lancet. 350 (9078), 630-633. Doi: 10.1016/​S0140-6736(96)08061-0
  
-Takeda (2012). Pathophysiology of COPD. http://​www.thinkcopdifferently.com/​About%20COPD/​What%20is%20COPD/​Pathophysiology%20of%20COPD.aspx+26. Takeda (2012). Pathophysiology of COPD. http://​www.thinkcopdifferently.com/​About%20COPD/​What%20is%20COPD/​Pathophysiology%20of%20COPD.aspx
    
-Tashkin, D. P., & Fabbri, L. M. (2010). Long-acting beta-agonists in the management of chronic obstructive pulmonary disease: current and future agents. Respiratory research, 11(1), 1.+27. Tashkin, D. P., & Fabbri, L. M. (2010). Long-acting beta-agonists in the management of chronic obstructive pulmonary disease: current and future agents. Respiratory research, 11(1), 1.
  
-Tests for COPD. (n.d.). NHS. Retrieved from http://​www.nhs.uk/​Conditions/​Chronic-obstructive-pulmonary-disease/​Pages/​Diagnosis.aspx+28. Tests for COPD. (n.d.). NHS. Retrieved from http://​www.nhs.uk/​Conditions/​Chronic-obstructive-pulmonary-disease/​Pages/​Diagnosis.aspx
    
-Van Noord, J. A., Aumann, J. L., Janssens, E., Smeets, J. J., Verhaert, J., Disse, B., ... & Cornelissen,​ P. J. G. (2005). Comparison of tiotropium once daily, formoterol twice daily and both combined once daily in patients with COPD. European Respiratory Journal, 26(2), 214-222.+29. Van Noord, J. A., Aumann, J. L., Janssens, E., Smeets, J. J., Verhaert, J., Disse, B., ... & Cornelissen,​ P. J. G. (2005). Comparison of tiotropium once daily, formoterol twice daily and both combined once daily in patients with COPD. European Respiratory Journal, 26(2), 214-222.
    
-Willemse, B. W. M., Ten Hacken, N. H. T., Rutgers, B., Lesman-Leegte,​ I. G. A. T., Postma, D. S., & Timens, W. (2005). Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers. European Respiratory Journal, 26(5), 835-845.+30. Willemse, B. W. M., Ten Hacken, N. H. T., Rutgers, B., Lesman-Leegte,​ I. G. A. T., Postma, D. S., & Timens, W. (2005). Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers. European Respiratory Journal, 26(5), 835-845.
  
-Willemse, B. W. M., Ten Hacken, N. H. T., Rutgers, B., Lesman-Leegte,​ I. G. A. T., Timens, W., & Postma, D. S. (2004). Smoking cessation improves both direct and indirect airway hyperresponsiveness in COPD. European respiratory journal, 24(3), 391-396.+31. Willemse, B. W. M., Ten Hacken, N. H. T., Rutgers, B., Lesman-Leegte,​ I. G. A. T., Timens, W., & Postma, D. S. (2004). Smoking cessation improves both direct and indirect airway hyperresponsiveness in COPD. European respiratory journal, 24(3), 391-396.
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